Internal Medicine

0521779407-09 CUNY1086/Karliner 0 521 77940 7 June 13, 2007 7:54

790 Hypomagnesemia

differential diagnosis

■Redistribution from extracellular to intracellular fluids:

➣Insulin administration post therapy of diabetic ketoacidosis,

hungry bone syndrome post parathyroidectomy, catecholamine

excess states such as ETOH withdrawal syndrome, acute pancre-

atitis, excessive lactation

■Reduced intake:

➣Starvation, alcoholism, prolonged postoperative state

■Reduced absorption

➣Specific GI magnesium malabsorption, generalized malabsorp-

tion syndrome, post extensive bowel resections, diffuse bowel

disease or injury, chronic diarrhea, laxative abuse

■Extra-renal factors that increase magnesuria

➣Drug-induced losses: Diuretics, aminoglycosides, digoxin, cis-

platinum and cyclosporine.

Hormone-induced magnesuria: Aldosteronism, hypoparathy-

roidism, hyperthyroidism.

Ion or nutrient-induced tubular losses: Hypercalcemia, extracellular

fluid volume expansion.

Miscellaneous causes: Phosphate depletion syndrome, alcohol

ingestion.

Hereditary causes of renal losses: Bartter’s and Gitelman’s syndrome;

familial hypomagnesemia with hypercalciuria/nephrocalcinosis (sec-

ondary to abnormalities in paracellin)

management

n/a

specific therapy

■Calcium ion is a direct antagonist of magnesium and should be given

to patients who are seriously ill with life-threatening magnesium

intoxication. Administer IV calcium as 100–200 mg of elemental cal-

cium over 5–10 min.

■Hemodialysis may be required following cessation of magnesium

therapy.

follow-up

n/a

complications and prognosis

n/a